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Query fever is caused by Coxiella burnetii, it’s a worldwide zoonotic infectious disease where domestic small ruminants are the main reservoirs for human infections. Coxiella burnetii, is a Gram-negative obligate intracellular bacterium, adapted to thrive within the phagolysosome of the phagocyte. Humans become infected primarily by inhaling aerosols that are contaminated with C. burnetii. Ingestion (particularly drinking raw milk) and person-to-person transmission are minor routes. Animals shed the bacterium in urine and feces, and in very high concentrations in birth by-products. The bacterium persists in the environment in a resistant spore-like form which may become airborne and transported long distances by the wind. It is considered primarily as occupational disease of workers in close contact with farm animals or processing their products, however, it may occur also in persons without direct contact. Doxycycline drug is the first line of treatment for Q fever. Treatment should be commenced immediately whenever Q fever is suspected. To prevent both the introduction and spread of Q fever infection, preventive measures should be implemented including immunization with currently available vaccines of domestic small ruminant animals and humans at risk. And controlling environmental contamination through the control of infected ticks and biosecurity measures may reduce introduction of C. burnetii to the farms. To sum up, the objective of this seminar paper is to give highlight on various aspects of Q fever in small ruminants with emphasis on its epidemiology, diagnosis, and its public health importance.
Q fever is a zoonotic disease caused by a unique intracellular bacterium Coxiella burnetii, which is a small obligate intracellular gram-negative bacterium that is prevalent throughout the world except in New Zealand and Antarctica . Recently, this intracellular bacterium was classified into the Legionellales order and the Coxiellaceae family . Infection with C. burnetii has been detected in humans and a wide range of animal species . The economic and public health impacts of Q fever remain a major concern in developing countries because Q fever causes significant loss of animal productivity and is a zoonotic risk to humans . Human infection, through the inhalation of contaminated aerosols, can cause a broad spectrum of presentations ranging from asymptomatic infection to life-threatening systemic infection. However, the consumption of milk and dairy products, skin contact, and person to person transmission is other routes of transmission of the infection . A small proportion of Coxiella burnetii infections are chronic and predominantly manifested as ‘endocarditis’ years after exposure. Interestingly, a recent study confirmed that, even with adequate antibiotic treatment, Q fever
has a significant long-term health impact with more than one in
three patients continuing to suffer from an impaired health status 24 months post-diagnosis .
Small ruminants are the primary reservoir for C. burnetii infection. Infection from these, predominantly dairy goats, and sheep, is generally subclinical. Although Coxiella can trigger abortion, the placenta and birthing fluid contains a substantial bacterial load that contaminates the local environment . Such contamination is a significant threat to both the agricultural industry and public health. This was recently demonstrated in the Netherlands where widespread Coxiella infection of goats, in a region of substantial goat farming, led to the largest Q fever outbreak ever recorded . During the period of 2007 and 2011, over 4000 human cases of Q fever were diagnosed in the Netherlands . The morbidity (the sickness) and mortality (the death) due to Q fever, in combination with the extremely low infectious dose and environmental stability of the agent, gave rise to the US Centers for Disease Control and Prevention classifying Coxiella burnetii as a biological weapon agent . Up to date, researchers are trying to investigate the molecular mechanisms of Coxiella burnetii pathogenesis which have been restricted by the obligate intracellular nature of Coxiella. However, the advent of a
pure sample of the organism in question has been grown, using
acidified citrate cysteine medium (ACCM), has transformed our
capacity to examine this unique pathogen .
Query fever infection has been described in most countries
except in New Zealand, Norway, Iceland and French Polynesia,
report that they have not found any evidence of this organism
in surveys to date. Q fever is transmissible to man in whom it is
characterized by sudden onset of fever, profuse sweating, chills,
anorexia, malaise, myalgia, and sometimes nausea and vomiting
etc. Most cases recover uneventfully but about 10 percent become
chronic developing endocarditis and occasionally pericarditis.
Cats, dogs, and wildlife may also serve as reservoirs hosts .
Coxiella burnetii has been identified in fish, rodents, wild
birds, horses, marsupials, swine, marine mammals, camels, ducks,
turkeys, geese, pets, and rabbits but was first isolated from a tick
and has been identified in ~40 species of tick subsequently. The
disease is subclinical in most animals, with adverse pregnancy
events reportedly the most common clinical sign. Abortion rates
can vary from a few cases up to 90% of the herd. In recent time C.
burnetii has been identified as a biological threat agent due to its
low infectious dose and high rate of transmission and is listed as a
group B bioterrorism agent by the CDC in the US . Few studies
are conducted in Ethiopia indicated that 6.5% seroprevalence of
C. burnetii was observed in Addis Ababa abattoir workers .
And, seroprevalence of 31.6%, 90%, and 54.2% of C. burnetii was
recorded in cattle, camels and goats respectively in South Eastern
Ethiopian pastoral zones of the Somali and Oromia regional states
Even if most animals are remaining totally asymptomatic,
including a lack of fever, low birth weight animals can occur .
Goats and sheep are the species in which abortions, stillbirths,
and early neonatal mortality have been most frequently
documented . Doxycycline drug is the first line of treatment of
Q fever for both animals and humans. Controlling environmental
contamination through the control of infected ticks and biosecurity
measures can reduce introduction of C. burnetii to the farms. Both
antibiotic treatment and vaccination are the methods available for
control and prevention of Coxiellosis. The objective of this seminar
paper is to give highlight on various aspects of Q fever in small
ruminants with emphasis on its epidemiology, diagnosis, and its
public health importance.
The aetiological agent of Q fever is Coxiella burnetii, which
is a Gram negative obligate intracellular bacterium, adapted to
thrive within the phagolysosome of the phagocyte. It has been
historically classified in the Rickettsiaceae family; however, recent
phylogenetic investigations, based mainly on 16s rRNA sequence
analysis, have shown that the Coxiella genus is distant from the
Rickettsia genus in the alpha subdivision of Proteobacteria .
Coxiella burnetii has therefore been placed in the Coxiellaceae
family in the order Legionellales of the gamma subdivision of
Proteobacteria. The complete genome sequencing of C. burnetii
has been achieved and confirms its systematic position. Unlike
rickettsiae family, Coxiella burnetii produces a small, dense, highly
resistant spore-like form .
In August 1935, Davis and Cox, after E.H., Derrick had isolated
in Queensland as the causative agent of Query fever, subsequently
found the same organism as that found by Derrick. Soon after
then, in 1939, the organism was named as Coxiella burnetii in
honor of Cox and Burnet, who had identified the organism as a
new Rickettsial . It is an intracellular organism which is a
polymorphic bacillus (0.2-0.4mm width, 0.4-1.0 mm length),
which has a cell membrane, like Gram negative bacteria .
However, it stains poorly with pigmented Gram stain, but gimenez
staining is traditionally used to stain the Coxiella burnetii pathogen
from pathological materials and crop .
Coxiella burnetii has several distinctive characteristics,
including a sporulation-like process that protects the organism
against the external environment, where it can survive for long
periods. In mammals, the usual host cell of C. burnetii is the
macrophage, which is unable to kill the bacterium. The other an
important characteristic of C. burnetii is its antigenic variations,
those called phase variation. This antigenic shift can be measured
and is valuable for differentiating acute from chronic Q fever .
Thus, it displays two antigenic phases those are phase-I and phase-
II that are liable to the Lipopolysaccharide (LPS) of the membrane.
Phase I Coxiella burnetii antigens are corresponds to the smooth
phase of Gram-negative bacteria and are more highly infectious
and phase-II antigen is corresponding to the granular (Rough)
phase which has a lower virulence. The strain of Coixella burnetii
pathogens are grouped into six (I VI) genomic group based on
the Restriction Fragment Length Polymorphism (RFLP). The
pathogenicity and the virulence of the C. burnetii are associated
with genetic characteristics, type of strains and plasmid groups
 and with host factors such as pregnancy .
Source, Maintenance and Transmission: Huge number of
animal species are susceptible to infection by C. burnetii including
ruminants, domestic carnivores, birds, wildlife mammals, and
arthropods, such as ticks. Various species may play a role in the
dissemination or maintenance of the disease, either as carriers or
as vectors of C. burnetii, although the role of some of the species
in the transmission of the disease has not been established with
certainty. The source of human infections cannot frequently be
established; however, sheep and goats are linked more frequently
to Query fever outbreaks in humans than are other animal species
Animal proximity and contact with infected animals and/
or their contaminated products (e.g. birth products) have been
identified as important risk factors for humans. In most outbreaks,
there are reports of spill-over of infection to humans from infected
domestic small ruminants, i.e. goats [27,28]. The bacterial shed
into the environment mainly occurs during parturition, during this period more than 109 bacteria are released at the time of
delivery. Goats mostly shed C. burnetii in vaginal mucus and milk,
whereas sheep shed mostly in feces . In goat’s duration of
shedding in milk is from several months to years. The udder and
retro-mammary lymph nodes may remain infected for more than
20 months. Goats can become chronically infected and may shed
for two consecutive C. burnetii pregnancies. Goats can shed C.
burnetii in also placenta and vaginal mucus during two or more
subsequent kidding. In contrast, ewes abort only one time, shed
C. burnetii in vaginal mucus during the abortion, but do not shed
in vaginal mucus at subsequent lambing . The duration of
excretion of C. burnetii may play a vital role in the persistence of
infection. Human incident cases are considered the best reflector
of disease activity globally, leading to intensified investigation into
Nevertheless, domestic small ruminants are considered the
main source of human infection because they may shed C. burnetii
in urine, feces, milk, and birth products. High concentrations of C.
burnetii are found in the placenta and vaginal secretions of infected
animals. Human infections occur after inhalation of aerosol or dust
particles with parturient fluids of infected animals. In addition,
bacterial survivability in adverse environmental condition and
long-term persistence as pseudo spores are likely to give rise to
the prevalence of enzootic-epizootic focus of Q fever .
Coxiella burnetii has been developed as a biological weapon.
Query fever is a potential biological warfare agent being very
infectious and very durable in the environment in a spore like form
as well as capable of windborne spread. In addition to this, another
route of transmission of C. burnetii could be through sabotage of
the food supply. Many scientific advances were made proving
that biological warfare was clearly feasible, although dependent
on careful planning, especially about meteorological conditions.
Large scale fermentation, concentration, purification, drying,
stabilization, and weaponization of pathogenic microorganisms
could be done safely.
In 1964, pathogens studied as biological weapons included
the agents causing: - Q fever, Anthrax, Glanders, Brucellosis, and a
variety of animal pathogens and plant . During the 1960s, bioweapon
developers in the U.S. considered Q fever as an excellent
“incapacitating” agent. The disease is debilitating, but rarely lethal.
The U.S. military envisioned using Q fever to cripple enemy forces
and drain them of resources .
The pathogenesis of C. burnetii infection in humans and
animals is not clearly understood. However, it is believed that
bacterial LPS play an important role in the pathogenesis of Q fever
in both animals and humans . The organism probably follows
the oropharyngeal route as its port of entry into the lungs and
intestine of both humans and animals . The disease is highly
infectious, and a very low dose is enough to initiate infection.
Primary multiplication takes place in the regional lymph nodes
after the initial entry, and a transient bacteraemia develops which
persists for five to seven days, as shown in sheep .
The bacteria C. burnetii has two morphologically distinct cell
variants: an intracellular, metabolically active Large Cell Variant
(LCV) and a spore-like Small Cell Variant (SCV). These two forms
are morphologically and functionally distinct. The LCV is larger,
elongated less electron-dense bacteria and metabolically active
and replicating by a large amount . While the SCV presents
a compact rod-shaped with a very dense central region, and it
is considered as the metabolically dormant and less replicating.
The SCVs are shed by infected animals. After infection the
organism attaches to the cell membrane of phagocytic cells. After
phagocytosis, the phagosome containing the SCV fuses with the
The SCVs are metabolically activated in the acidic
phagolysosome and can undergo vegetative growth to form LCVs
[38,39]. The LCVs and the activated SVCs can be divided by binary
fission and they can also undergo saprogenic differentiation. The
spores that are produced can undergo further development to
become metabolically inactive SCVs , and both spores and SCVs
can then be released from the infected host cell by either cell lysis or
exocytosis. The entire developmental cycle of metabolically active
Coxiella burnetii takes place in acidic phagolysosome, C. burnetii is
resistant to microbicidal activities in the host macrophages. The
acidic environment also protects C. burnetii from the effects of
antibiotics, as the efficacy of antibiotics is decreased in the acidic
pH. The SCV and spore forms are more difficult to denature than
LCVs , possibly due to differences in cell wall composition and
thickness as well as water content.
In Small Ruminants: Coxiellosis in livestock species is
generally asymptomatic. In animals, during the acute phase,
C. burnetii can be found in the blood, spleen, lungs, and liver
whereas during the chronic phase it is presented as a persistent
shedding of C. burnetii in urine and feces. Most animals remain
totally asymptomatic, including a lack of fever. However, low
birth weight animals can occur. Goats and sheep are the species
in which abortions, stillbirths, and early neonatal mortality have
been most frequently documented. In many cases, abortion occurs
in late pregnancy which range from 3 to 80% with unspecified
characteristic clinical signs of infection with C. burnetii.
Temperature is an important factor related to abortion rates
in herds, since fewer abortions take place between months of
November and December. However, the occurrence of abortion
rate increases gradually from January to February, decreasing
again in March. The Aborted fetuses appear normal but, infected
placentas exhibit intercotyledonary fibrous thickening and
discolored exudates, which are not specific to Q fever . A
severe inflammatory response is noted in the myometrium of
goats and goats shed C. burnetii in feces before and after kidding
and the mean duration of excretion is 20 days. C. burnetii can also
be recovered from milk for up to 32 months.
In Humans:Coxiella burnetii infection can cause either an
asymptomatic, acute, or chronic disease. Size of the inoculums,
route, and duration of exposure, as well as host factors influence
the duration of the incubation period and may contribute to the
clinical expression of acute and chronic clinical disease. Monocytes
and macrophages are the primary target cell . Inhalation of
aerosolized bacteria through the respiratory tract is the Primary
route of infection, with alveolar macrophages being targeted.
Kupffer cells of the liver are affected through bacteremia or, rarely,
digestive route exposure. Only 4% of those affected with acute
Q fever need hospitalization for their symptoms. The incubation
period prior to acute clinical Q fever is estimated at approximately
20 days (range: 12 to 39 days)  depending on inoculating dose
The mean incubation period between the onset of clinical
signs and acute Q fever diagnosis is estimated at 2 months. Acute
Q fever is seen as a self-limiting mild febrile illness and may be
associated with headache, myalgia, arthralgia, and coughing .
Prolonged fever is usually accompanied by severe headaches
may reach from 39 to 40.8 °C, usually remaining elevated all
day. Fever typically increases to plateaus within 2-4 days and
returns to normality within 5-14 days in treated individuals.
Untreated patients may observe fever of 5-57 days duration.
Atypical pneumonia is one of the most commonly recognized
forms of acute Q fever. Most cases are clinically asymptomatic or
mild, characterized by a nonproductive cough, fever, and minimal
auscultatory abnormalities, but some patients present with acute
respiratory distress .
Hepatitis is also commonly observed, which is usually
accompanied clinically by fever and less frequently by abdominal
pain, anorexia, vomiting, nausea, and diarrhea. Advanced icterus
and palpation of a mass in the right hypochondrium have also been
reported. Rarely, dermatological and neurologic manifestations
occur . The annual mortality rates in the general population
associated with acute clinical Q fever range from 0.9 per 100,000
per year in the United Kingdom to 2.4 per million per year in
France (Figure 1). Myocarditis is the leading cause of death in
acute disease and accounts for 2% of all clinical cases .
Acute disease does not have to precede chronic Q fever. Five
percent (5%) of chronic Q fever occurs in infected individuals 
and is characterized by persistent infection beyond six months. It
happens almost exclusively in high risk patients, including those
with immunosuppression, vascular abnormalities, heart valve
lesions, and pregnancy. The prognosis of Q fever is very poor, if it is
not treated . Clinical indications of prolonged persistence of Q
fever (chronic Q fever) include; osteo-articular infections, chronic
hepatitis, infection of the ventriculo-peritoneal drain , pseudo
tumors of the spleen and lung , and chronic fatigue syndrome
. In general sense, the clinical signs in human are the ones
listed below: Rash, Pregnancy (week by week, trimesters),
Headache, Diarrhea, Abdominal Pain, Pneumonia, Influenza like
syndrome, Meningoencephalitis, Hepatitis, Endocarditis, etc.
Collection of Samples: In the acute-phase of the disease,
immediately serum sample should be collected after the onset
of symptoms (within the first 2 weeks) with a convalescentphase
specimen collected 3–6 weeks later. Before antibiotic
administration the whole blood should be collected in EDTAtreated
anticoagulant tubes and shipped refrigerated on the
frozen gel packs by overnight. The Buffy coat can be saved for
DNA amplification and stored frozen in a non–frost-free freezer
if samples are to be prepared for other laboratory tests. The most
commonly evaluated sample used for confirmation for chronic Q
fever is heart valve tissue. If the fresh samples being transported
within 24 hours they should be refrigerated and shipped on frozen
gel packs. However, if the transport does not occur within 24
hours, it should be frozen in a non–frost-free freezer and shipped
on dry ice for either culture or PCR analysis .
Staining and Related Measures: The diagnosis of coxiellosis
in aborted small ruminants by an ordinary method is to detect
the pathogen using staining techniques. The smears prepared
from the samples are usually stained by Gimenez, Stamp, Giemsa
stain or Machiavello. Strong presumptive diagnosis of C. burnetii
is indicated by the presence of large masses of red-colored
coccobacilli. Due to possible confusion with other pathogens
such as Brucella species or Chlamydia species, these diagnostic methods are poorly sensitive and not specific for Q fever . This
is followed by a serological analysis by the CFT, or better by ELISA
. However, staining techniques cannot be specific and they
have reduced sensitivity, especially with vaginal swabs, milk and
a fecal sample.
Isolation and Cultivation: For routine diagnosis of Q fever
cultivation of C. burnetii is not recommended, since the process
is very difficult, time consuming, and dangerous. In addition
to this culture of C. burnetii requires a bio-safety level 3 (BSL-
3) laboratory because bacteria are highly infective and can be
hazardous for laboratory workers. Patients with chronic Q fever
have already received antibiotics which can further complicate
isolation attempts; a negative culture does not rule out a C. burnetii
infection. Specimens can be referred to CDC through state public
health laboratories for culture.
Serology: The commonest serological tests presently used
for the diagnosis of C. burnetii in animals are the compliment
fixation test (CFT), immunofluorescence assay (IFA) and enzyme
linked immunosorbent assays (ELISA) . The CFT has lower
sensitivity as a diagnostic test for Q-fever compared to IFA and
ELISA tests which are highly specific and sensitive to both phase
I and phase II antigens . Both IFA and ELISA tests were used
in the present study and compared as herd screening tests. The
IFA assays employ fluorescent markers conjugated to a specific
antibody to detect antigen-antibody (Ag: Ab) reaction. In positive
cases, the fluorescent marker in the Ag: Ab complex emits a green
light which is detected under the fluorescent microscope. The
two available tests for serological diagnosis of Q fever are direct
and indirect types of test. The latter is the one more commonly
used. On the other hand, the most commonly used ELISA assay
for screening C. burnetii infection in ruminants is an indirect test
which utilizes a horseradish peroxidase-labeled monoclonal antiruminant
IgG conjugate that reacts with a wide range of domestic
and wild ruminant species  (Figure 2).
Molecular Method: For study transmission routes, and
to assess sources of infection of C. burnetii, molecular typing of
pathogenic microorganisms is mainly important. Use of antibiotics
and vaccination may interfere with the structure of bacterial
populations and this can be evaluated by comparing molecular
typing profiles of members of these populations. The prerequisite
for surveillance purposes and epidemiological investigation of Q
fever outbreaks is genotypic characterization of C. burnetiid .
Two PCR C. burnetii typing methods have been described. Those
are 1, Multi-Locus Variable number of tandem repeats Analysis
(MLVA) and 2, Multispacer Sequence Typing (MST) that permit the
typing of C. burnetii without the need for isolation of the organism
Multispacer Sequence Typing, depending on DNA sequence
variations in10 short intergenic regions, can be performed on
isolated C. burnetii strains or directly on extracted DNA from
clinical samples. To date, the most discriminating methods for
C. burnetii those allowing the identification of up to 36 distinct
genotypes are MLVA and MST. The availability of such databases
allows inter-laboratory comparisons to be made easily and this
will lead to a better understanding of the propagation of the C.
burnetii isolates. Furthermore, their use in the characterization of
field samples or isolates is increasing .
The disorders for which we appreciate the same signs with
that of Q fever are: Elective Abortion, Influenza, and Rickettsial
Infection. At initial stages, i.e., before pulmonary symptoms are
present, influenza may be suspected. Furthermore, Salmonellosis,
Brucellosis, Leptospirosis, Campylobacteriosis, and less severe
disease due to Rickettsial species should be included in differential
diagnosis. Malaria and Dengue should have to be excluded,
especially in tropical areas .
Query fever is essentially an airborne disease which is caused
by C. burnetii. Human infections occur after inhalation of aerosols generated from infected placentas, body fluids or contaminated
dust resulting from contaminated manure and desiccation of
infected placenta. Transmission of C. burnetii is mostly associated
with abortion of domestic small ruminants, and particularly with
ovine abortions. Seasonal variation in the incidence of the human
disease in the spring and early summer IS described by a several
authors which has been attributed to spring lambing and shearing
which in turn leads to environmental contamination .
Indeed, people may be infected by handling contaminated
wool, manure or clothes contaminated with feces or transhumance
of infected flocks through a valley . Then direct contact with
aborted females is not required. In addition, between June and
November 2002, in the Chamonix valley in France, 88 human
cases of Q fever did identify, 71 with clinical signs and 10 need
hospitalizations. The origin of this outbreak due to airborne
transmission from some infected flocks present in the valley
since then. In the USA, C. burnetii is enzootic in wild animals and
ruminants as in other parts of the world, but human infections
due to C. burnetii are rare . Certain cases of Q fever have been
described in Australia , Canada , France, Germany ,
Japan , Spain, Switzerland and the United Kingdom .
Except in Bulgaria where the rise of the number of goats that
daily go through villages and small towns for grazing is associated
with an increase in human Q fever, a few information is available
to explain such an increase of cases of Q fever . A recent study
has also confirmed that, Q fever has a significant long-term health
impact with more than one in to 24 months post diagnosis. Since
the multiple forms of the disease hinder its clinical diagnosis, the
prevalence of Q fever in humans as well as in animals is not known
accurately and is probably underestimated. The existence of C.
burnetii in the environment allows it to be disseminated by wind
far away from its original source. This indicate the appearance of
Q fever cases in urban areas, where an important percentage of
patients fails to report direct contact with animals .
Apparently without animal contact, domestic and wild birds
can also be responsible for human cases in urban areas since they
are able to transmit Q fever via their feces or their ectoparasites.
The airborne transmission of C. burnetii associated with its highly
resistance to environments and the ability to easily produce
huge quantities of C. burnetii in the after birth of aborted ewes
or goats have led to classify C. burnetii as a category-B, biological
terrorism agent . Then it was perhaps used for this purpose
during World War II. The classification C. burnetii under biological
terrorism agent has been responsible for the publication of several
reviews on Q fever.
The attention of public health personnel and medical on Q
fever, which could be responsible for the apparent increase of Q
fever cases and its apparent reemergence, has been focused. Less
efficient route of contamination is ingestion of contaminated raw
milk or raw milk products. Without clinical signs, seroconversion in
human volunteers has been induced by drinking of contaminated
milk, but none of them presented aggravating risk factors.
Nevertheless, some studies have reported clinical disease linked
to the ingestion of cheese; but these outcomes are sometimes
contested since it is difficult to guarantee even for prisoners that
the patients did not inhale contaminated dust or aerosols .
Treatment is indicated for all infections, even for those that are
subclinical. For domestic small ruminants’ oral therapeutic dose
may be given for 24 weeks . Doxycycline is the first choice of
drugs treatment for all adults, and children those have severe
illness. Treatment should be initiated immediately whenever
Q fever is suspected. The other use of antibiotics other than
doxycycline for 14 to 21 days at a dosage of 100 mg twice daily
to adults and 2.2mg/kg body weight twice daily to children under
45kg or other tetracycline, at a dose 8mg/kg in drinking water,
several weeks before lambing, was recommended as a possible
prevention protocol is also associated with a higher risk of severe
For preventing the development of severe complications,
doxycycline is most effective if it is treatment started earlier
in the course of disease. In some cases, such as, survival in
endovascular complications such as mycotic aneurysm or vascular
graft infections surgical intervention may be necessary. Surgical
debridement is also prescribed for osteo-articular infections.
After the fever subsides patients should be treated for at least 3
days until there is evidence of clinical improvement. As stated by
CDC , the standard duration of treatment is 2-3 weeks .
Children who is less than 8 years of age with mild illness should
be treated with cotrimoxazole, but therapy should be switched
to doxycycline if their course of illness worsens. Trimoxazole
treatment of pregnant women diagnosed with acute Q fever with
once daily throughout pregnancy significantly decreases the
risk of adverse consequences for the fetus. In adults 100 mg of
doxycycline in every 12 hours and 200mg of hydroxychloroquine
in every 8 hours is indicated for Chronic Q fever. Standard duration
of treatment is 18 months .
The best methods available for prevention and control of
Coxiellosis are antibiotic treatment and vaccination. In-feed
addition of tetracycline or injectable oxytetracycline pre-partum
has not been shown to prevent C. burnetii shedding in feces, milk
and vaginal secretions . Due to the lack of enough evidence
that supporting antibiotic efficacy and the fact that prudent use of
antibiotics is needed to avoid resistance, they should not be used
for treatment of Q fever in animals at this time.
Vaccination with a phase-I C. burnetii, inactivated vaccine is
reportedly effective for abortion prevention, and the reduction of
bacterial shedding in goats and sheep  and is most effective in
primiparous animals. If animal is already infected with C. burnetii
vaccination may not be effective . In Australia, phase-I vaccine
is currently available for human use and has been recommended
for high risk, occupationally exposed, sero negative individuals.
Great attention should be given to C. burnetii since it can survive
for several weeks outside a host in warm, moist environments.
Bearing in mind small ruminants as the main reservoirs,
controlling endemic Coxiellosis in herd may play a crucial role in
reducing disease in populations living in close contact with infected
animals (Table 1). Controlling environmental contamination
through the control of infected ticks and biosecurity measures
may reduce introduction of C. burnetii to the farms. The preferred
method for handling manure and bedding and decreases the
Coxiella burden and risk of spread is composting .
During transport of manure it should be covered, stored in a
location where water run-off and water contamination is minimal.
To reduce the risk of spread through aerosolization, transport
and spread of manure should be done when wind is minimal .
Composting carcasses and aborted tissues and contaminated
bedding on site is preferred . Vaccination offers a new
conception of suppression and eradication of this Zoonosis, not
only in a view of public health safety but also in creating Q fever
free regions in endemic areas .
As a few studies conducted in Ethiopia indicated that 6.5%
seroprevalence of C. burnetii was observed in Addis Ababa abattoir
workers. Also, the existence of antibody against C. burnetii was
reported in goats and sheep slaughtered at Addis Ababa abattoir,
and its peri-urban zones . A seroprevalence of 31.6%, 90%,
and 54.2% of C. burnetii was recorded in cattle, camels and
goats respectively in South Eastern Ethiopian pastoral zones of
the Somali and Oromia regional states. Ticks were tested for C.
burnetii in Ethiopia by quantitative real time polymerase chain
reaction targeting two different genes followed by multispacer
sequence typing (MST). An overall prevalence of 6.4% of C. burnetii
was recorded. C. burnetii was detected in 28.6% of Amblyomma
gemma, 25% of Rhipicephalus pulchellus, 7.1% of Hyalomma
marginatum rufipes, 3.2% of Amblyomma variegatum, 3.1% of
Amblyomma cohaerens, 1.6% of Rhihipicephalus praetextatus,
and 0.6% of Rhipicephalus (Boophilus) decoloratus. Significantly
higher overall frequencies of C. burnetii DNA were observed in
Amblyomma gemma and Rhihipicephalus pulchellus than in other
tick species .
Coxiellosis (Query fever) is a zoonotic disease caused by an
obligate intracellular bacterium known as C. burnetii. This disorder
has repeatedly been described since the 1930s and cannot be
defined yet as an emerging zoonotic disease. Re-emergence of
this case could be explained by the improvement of the diagnosis
for which serological tests and PCR allow an accurate detection of
the infected flocks [90,91]. The high prevalence of acute Q fever
could reflect such vigilance even if the mandatory notification
of Q fever by physicians, veterinarians and laboratories does
not exist wherever it has been undertaken. This tells us that
mandatory notification is not always the accurate solution for a
better knowledge of its epidemiology. Nowadays, this measure
is not desirable in veterinary medicine until more data on the
disease become available in order to propose validated methods
to efficiently prevent the transmission of the disease to humans.
In order to precisely identify the origin of each human infection
and to better understand the mechanisms paving a way to various
clinical manifestations in humans and small ruminants, in fact,
it is necessary to obtain more data on the bacteria, on molecular
markers and virulence factors.
As it has been tried to be mentioned in the above review,
most of the outbreaks of Q fever in humans are related to goats
and sheep, but until now it has not been identified whether or not,
the C. burnetii isolated from sheep are more virulent than those
isolated from goats and any others, or why sheep preferentially
shed C. burnetii in vaginal mucus and feces, whatever the virulence
of the strain could be. Furthermore, the efficiency of antibiotic
treatments in small ruminants on bacterial shedding must be well
evaluated. To conclude, it is advisable to inform the persons at
risk: farmers, veterinarians, livestock workers, immunodeficient
patients or those suffered from cardiac valvopathy and pregnant
women that they must avoid contact with ewes and goats during
delivering their lambs and kids, even cows during delivery period.
Based on the above conclusion the following measures should
be taken into account for prevention; control and management of
Q fever as far as all above characters are concerned:
a. Lambing and kidding areas should be regularly cleaned
and disinfected to prevent accumulation of potentially
contaminated materials and it is preferable that birthing
should occur indoors away from the wind.
b. Be sure that the placenta and fetus from aborted goats
and sheep are submitted for examination to an accredited
veterinary diagnostic laboratory in order to test for C. burnetii.
Because, placenta is the key sample to submit since the
organism may not be detectable in the fetus.
c. All personal hygienic measures should be taken into
consideration and every livestock owner should manage his
own herd in well applicable manner.
d. Pregnant women and highly at-risk person should not
assist, even should avoid contact in lambing or kidding; infants
and young children, the elderly and immunocompromised
persons should be given care.
e. Mammals, in effect, domestic small ruminants should
be immunized through vaccination which is effective for
controlling infection and transmission since there is no
practical means for eradication of C. burnetii from the
f. Further research should be conducted regarding Q fever
in small ruminants in Ethiopia so that it may help in designing
the mitigating approaches.